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1 (PLA2R1) is the major autoantigen in primary membranous nephropathy.
2 lie the loss of podocyte barrier function in membranous nephropathy.
3 eymann nephritis (PHN), a rat model of human membranous nephropathy.
4 ce active Heymann nephritis (HN), a model of membranous nephropathy.
5 Heymann nephritis (HN), a rat model of human membranous nephropathy.
6 glomerulonephritis and less frequently with membranous nephropathy.
7 tients met the criteria for NSAID-associated membranous nephropathy.
8 AID intake should be sought in patients with membranous nephropathy.
9 A2R1) is the major autoantigen in idiopathic membranous nephropathy.
10 toantigen in 70% of patients with idiopathic membranous nephropathy.
11 y showed phospholipase A 2 receptor-negative membranous nephropathy.
12 he UPS depended on oxidative modification in membranous nephropathy.
13 imal-change disease and a low correlation in membranous nephropathy.
14 d human glomerular diseases, particularly in membranous nephropathy.
15 rtant advances regarding the pathogenesis of membranous nephropathy.
16 R) is the major target antigen in idiopathic membranous nephropathy.
17 R) are sensitive and specific for idiopathic membranous nephropathy.
18 dict response to treatment with rituximab in membranous nephropathy.
19 and segmental glomerulosclerosis (FSGS) and membranous nephropathy.
20 mmune deposits in glomeruli of patients with membranous nephropathy.
21 peutic intervention in patients with primary membranous nephropathy.
22 erlying disease and seems to be greatest for membranous nephropathy.
23 diseases, with highest induction observed in membranous nephropathy.
24 omerulonephritis, and severe skin lesions or membranous nephropathy.
25 Here, we describe a patient with recurrent membranous nephropathy 13 days after kidney transplantat
29 n the prominent expression of FHR-5 in human membranous nephropathy, a disease in which complement ac
30 (18-75 years) with biopsy-proven idiopathic membranous nephropathy, a plasma creatinine concentratio
31 g a large cohort of patients with idiopathic membranous nephropathy according to a restrictive treatm
32 steroid-sensitive nephrotic syndrome or with membranous nephropathy after transplantation had low lev
34 For the subset of patients with idiopathic membranous nephropathy and deteriorating excretory renal
38 rt of 117 Caucasian patients with idiopathic membranous nephropathy and nephrotic-range proteinuria u
42 e glomerulonephritis and another patient had membranous nephropathy as the cause of end-stage renal d
43 been made in our understanding of idiopathic membranous nephropathy, as well as treatment of this dis
44 (St-Cp) therapy for patients with idiopathic membranous nephropathy at high risk of progression to ES
46 - was induced in minimal change disease and membranous nephropathy, but not focal segmental glomerul
47 om such deposits in patients with idiopathic membranous nephropathy, but not in those with lupus memb
48 A2R is the target of the autoimmune disease, membranous nephropathy, characterised by production of a
50 given sheep anti-Fx1A to induce experimental membranous nephropathy; control rats received normal she
51 r cohort, 15 of 154 patients with idiopathic membranous nephropathy had circulating autoantibodies to
54 rulosclerosis (HR, 0.80; 95% CI, 0.77-0.82), membranous nephropathy (HR, 0.88; 95% CI, 0.83-0.93), me
55 nephropathy (HRa, 0.74; 95% CI, 0.59-0.92), membranous nephropathy (HRa, 0.47; 95% CI, 0.29-0.75), a
56 ase were primary FSGS, diabetic nephropathy, membranous nephropathy, immunoglobulin A nephropathy, an
61 phritis is an experimental model that mimics membranous nephropathy in humans, wherein the glomerular
62 in seven patients, diabetic nephropathy and membranous nephropathy in one patient, and death due to
65 peutic advances for patients with idiopathic membranous nephropathy, including antibody inhibition th
66 immune deposits in patients with idiopathic membranous nephropathy, indicating that PLA(2)R is a maj
77 d decline in renal function in patients with membranous nephropathy may be due to renal vein thrombos
78 actors, compared with IgAN (referent), FSGS, membranous nephropathy, membranoproliferative GN, lupus
79 ed as a surrogate for long-term prognosis in membranous nephropathy (MGN), variability in proteinuria
80 D7A) is a target antigen identified in adult membranous nephropathy (MN) along with the major antigen
81 Absent a remission of proteinuria, primary membranous nephropathy (MN) can lead to ESRD over many y
83 he Heymann nephritis (HN) rat model of human membranous nephropathy (MN) have shown that IgG antibodi
84 fies a new antigen responsible for secondary membranous nephropathy (MN) in a patient with mucopolysa
90 As recently as 2002, most cases of primary membranous nephropathy (MN), a relatively common cause o
91 A) are the two major autoantigens in primary membranous nephropathy (MN), and define two molecular su
92 ssion in two-thirds of patients with primary membranous nephropathy (MN), even after other treatments
93 is (FSGS), minimal change disease (MCD), and membranous nephropathy (MN), may respond well to cyclosp
95 erosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MNP], lupus nephritis [LN], and
96 vs IgAN, ranged from 0.49 for DN to 0.92 for membranous nephropathy or ADPKD) than by lower rates of
97 and nephrotic syndrome caused by idiopathic membranous nephropathy or focal segmental glomeruloscler
98 s from patients with idiopathic or secondary membranous nephropathy or other proteinuric or autoimmun
102 ive glomerulonephritis, IgA nephropathy, and membranous nephropathy), patients with systemic lupus er
103 serum samples from patients with idiopathic membranous nephropathy, patients with other glomerular d
106 correlate with the immunological activity of membranous nephropathy, potentially exhibiting a more ra
107 cohort with anti-PLA2R1-negative idiopathic membranous nephropathy recognized a glomerular protein t
111 ents (70%) with idiopathic but not secondary membranous nephropathy specifically identified a 185-kD
112 lomerulopathies minimal-change nephrosis and membranous nephropathy, there is an increase in Shp2 pho
113 use of immunosuppressive drugs in idiopathic membranous nephropathy to patients at the highest risk o
114 of immune deposit formation in experimental membranous nephropathy to the role of a microRNA in FSGS
116 with a nephrotic syndrome and biopsy-proven membranous nephropathy were administered a 3 to 6-month
117 while taking an NSAID and if other causes of membranous nephropathy were excluded and a rapid remissi
118 tibodies in serum samples from patients with membranous nephropathy were mainly IgG4, the predominant
119 were serially evaluated in 15 patients with membranous nephropathy who exhibited relapsing nephrosis
121 samples from the 74 patients with idiopathic membranous nephropathy who were seropositive for anti-PL
122 pholipase A(2) receptor-associated recurrent membranous nephropathy with circulating anti-Phospholipa
123 s renal function in patients with idiopathic membranous nephropathy with declining renal function.
124 a kidney transplant and developed recurrent membranous nephropathy with fine granular co-localizatio
125 y in this cohort of patients with idiopathic membranous nephropathy yielded favorable outcomes while
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